Role of adenosine or AMP as a probable mediator of blood flow regulation in canine hindlimb muscles.

Canine hindlimb muscles were perfused with arterial blood from a donor at a constant pressure or at a constant flow rate. Blood samples were analyzed for adenosine, oxygen and potassium during load-free twitch contractions (2 cps) and/or after 3-min ischemia. (1) During exercise hyperemia A-V oxygen (p smaller than 0.001) and V-A potassium (p smaller than 0.001) differences increased in both perfusion systems. Under the constant pressure total amount of adenosine and/or AMP released (TAAR) remained constant at 34.4 plus or minus 7.8 (mean plus or minus S.D.) nmoles/ml of blood compared with 31.0 plus or minus 5.6 at rest, whereas under the constant flow rate the value increased from 32.8 plus or minus 9.4 to 74.6 plus or minus 15.7 (p smaller than 0.001). (2) In reactive hyperemia A-V difference of oxygen increased (p smaller than 0.001) and TAAR remained at 33.0 plus or minus 8.3 under the constant pressure. Under the constant flow rate TAAR increased from 32.8 plus or minus 9.4 to 48.1 plus or minus 12.6 (p smaller than 0.001). (3) After ischemic contractions TAAR remained constant under the constant pressure perfusion. Under the constant flow rate, however, TAAR showed definite decrease compared with that during exercise hyperemia with intact flow (p smaller than 0.001). (4) The authors think that adenosine and/or AMP is the mediator of exercise hyperemia, supported by potassium ions and local hypoxia. Adenosine and/or AMP, and local hypoxia are responsible for reactive hyperemia. In ischemic contractions, no special circulatory mediator was found.